Coronary heart disease is generally thought to be caused by the narrowing of coronary arteries by atherosclerosis, which includes the buildup of fatty deposits in the lining of the arteries. The process that may lead to atherosclerosis begins with the accumulation of excess fats and cholesterol in the blood. These substances infiltrate the lining of arteries, gradually increasing in size to form deposits commonly referred to as plaque or atherosclerotic occlusions. Plaques narrow the arterial lumen and impede blood flow. Blood cells may collect around the plaque, eventually creating a blood clot that may block the artery completely.
The phenomenon of “vulnerable plaque” has created new challenges in recent years for the treatment of heart disease. Unlike occlusive plaques that impede blood flow, vulnerable plaque develops within the arterial walls, but it often does so without the characteristic substantial narrowing of the arterial lumen which produces symptoms. As such, conventional methods for detecting heart disease, such as an angiogram, may not detect vulnerable plaque growth into the arterial wall. After death, an autopsy can reveal the plaque congested in the arterial wall that could not have been seen otherwise with currently available medical technology.
The intrinsic histological features that may characterize a vulnerable plaque include increased lipid content, increased macrophage, foam cell and T lymphocyte content, and reduced collagen and smooth muscle cell (SMC) content. As shown in FIG. 1A, this fibroatheroma type of vulnerable plaque 101 is often referred to as “soft,” having a large lipid pool 102 of lipoproteins surrounded by a fibrous cap 103. The fibrous cap 103 contains mostly collagen, whose reduced concentration combined with macrophage derived enzyme degradations can cause the fibrous cap of these lesions to rupture under unpredictable circumstances. When ruptured, as shown in FIG. 1B, the lipid core contents, thought to include tissue factor, contact the arterial bloodstream 104, causing a blood clot 105 to form that can completely and very quickly block the artery (e.g., lumen 106) resulting in an acute coronary syndrome (ACS) event. This type of atherosclerosis is coined “vulnerable” because of the unpredictable tendency of the plaque to rupture. It is thought that hemodynamic and cardiac forces, which yield circumferential stress, shear stress, and flexion stress, may cause disruption of a fibroatheroma type of vulnerable plaque. These forces may rise as the result of simple movements, such as getting out of bed in the morning, in addition to in vivo forces related to blood flow and the beating of the heart. It is thought that plaque vulnerability in fibroatheroma types is determined primarily by factors which include: (1) size and consistency of the lipid core; (2) thickness of the fibrous cap covering the lipid core; and (3) inflammation and repair within the fibrous cap.
Some physicians have stated that rupture of a vulnerable plaque during a PTCI (percutaneous transluminal coronary intervention) is desirable. The rationale is that if a rupture is going to occur, it is better to have it happen in the safety and security of the catheterization lab. In this way, an immediate corrective action can be taken to deal with the plaque rupture. It has been further stated that it may be desirable to have the lipid pool under the fibrous cap completely drained to prevent a blood clot build up. Therefore, it is desirable to have a device which will ensure rupture of the fibrous cap during the intervention.